The Eastern European experience on occupational skin diseases. Make underreporting an issue?

BACKGROUND: While legislation in most of the Eastern European countries is nowadays widely harmonized with the legal safety and health provisions of Western countries, there is still a sustained resistance to the notification of occupational skin diseases (OSD). OBJECTIVE: The aim of the study was to identify the main barriers in notification and recognition of OSD in 22 Eastern European countries. METHODS: An online survey was administered to key persons in the field of occupational safety and health in 22 Eastern European countries. Multiple variables of the notification system were studied, including clinical, organizational and educational issues. RESULTS: The main causes of underreporting OSD are ineffective enforcement of occupational safety and health legislation, contractual relationship employer-employee, long duration of the notifying process, restrictions of the notification systems in terms of who is entitled to notify an OSD, ineffective regulations in regards to the pre-employment and periodical medical examination, ineffective compensation schemes, restraints and hesitations, mainly from the doctors, inappropriate mentalities - fear of losing the jobs, fining of the employers by the authorities, stigmatization of the workers with OSD, additional costs for employers, stakeholders' lack of interest in notifying, lack of guidelines and protocols and lack of preventive programmes. CONCLUSIONS: The most valuable method for a proper recognition of OSD is to increase the awareness of physicians involved in the management of OSD (occupational physicians, GPs, dermatologists), as well as employers and workers. There is an urgent need to improve national legislation, to develop and promote adequate preventive programmes, emphasizing ethical, legal, economical and psychological aspects in order to achieve an increased recognition and a real reporting of OSD, and to enforce an international action plan for Eastern Europe in order to improve the notification of OSD.

Anatomo-clinical analysis of 14 consecutive cases of primary cystic mesenterico-epiploic tumors.

BACKGROUND: The aim of this study is an anatomo-clinical evaluation of the primary cystic mesenterico-epiploic tumors,based on a single-center's 15 year experience. MATERIAL AND METHOD: We performed a retrospective study of a series of 14 primary cystic mesenterico-epiploic tumors that were operated in the Surgical Department 4 UMPh Targu-Mures, Romania, between 01.01.1997 and 01.01.2012. Data about the clinical complaints, imagistic aspects, associated lesions, surgical approach, hospitalization, pathology, and immediate and late postoperative course were recorded and analysed using the Microsoft Excel software. RESULTS: In all cases we performed a complete and intact surgical excision, using an open approach in 13 cases and laparoscopy in 1 case, with no mortality and no significant surgical-related morbidity; we have encountered a single recurrence at 1.5 years after surgery. We had no preoperative pathological diagnosis; the exact preoperative anatomic location of the tumor was possible only in one case. Pathologic examination showed the following types: inclusion cysts - 4 cases, enteral duplication cysts - 2 cases, simple mesothelialcysts - 6 cases, cystic lymphangioma - 1 case and simple lymphatic cyst - 1 case. We have systematized 3 clinicoimagistic patterns according to the dimension of the tumor,with no relationship to the histologic origin of the tumor. CONCLUSIONS: Primary cystic mesenterico-epiploic tumors aredifficult to diagnose preoperatively. Complete excision is usually possible, even for large tumors. These relatively rare tumors must be considered in the differential diagnosis of cystic abdominal masses.

[Effect of pancreatin replacement on pancreatic function in the postoperative period after pancreatic surgery]. / Pankreatin-kezelés hatása a pancreasfunkcióra hasnyálmirigymütétek utáni posztoperatív periódusban.

There is evidence that disturbances of exocrine function can persist for several weeks following pancreatic surgery. Active proteases in the duodenal lumen may help to recovery of exocrine function. A placebo-controlled trial of enteric-coated pancreatin (25,000 U lipase; 3 x 1 caps/day) was performed during 2 weeks following pancreatic surgery (resection and drainage operation). A total of 39 patients were randomized, 20 to pancreatin group and 19 to placebo group. The exocrine function was tested via serum and faecal elastase determinations, the amylum tolerance test (ATT) and checks on the symptoms of maldigestion. After medication for 10 days, there was evidence of the beneficial effect of pancreatin suggested by a 35% improvement in ATT, an unchanged body weight and the disappearance of symptoms of maldigestion. In the control group, abnormal ATT and symptoms of maldigestion were remained, while the body weight decreased with by 3.5 kg. In both groups, no significant change was noted in the elastase concentration. The results suggest that enteric-coated pancreatin treatment after pancreatic surgery may lead to a rapid improvement of exocrine pancreatic function, probably by reducing the cholelcystokinin response to stimulation by food and represent a new indication of the enteric-coated pancreatin medication.

Beneficial effects of pentoxifylline treatment of experimental acute pancreatitis in rats.

UNLABELLED: The purposes of this study were to determine the tumor necrosis factor (TNF) and interleukin-6 (IL-6) levels after the induction of acute necrotizing pancreatitis, and to establish the effects of pentoxifylline on cytokine production. METHODS: acute pancreatitis was induced by the retrograde injection of 200 microliters taurocholic acid into the pancreatic duct in male Wistar rats. The serum amylase activity, the wet pancreatic weight/body weight ratio, and the TNF and IL-6 levels were measured. Seven mg/kg pentoxifylline were administered intraperitoneally at the time of operation 6, 12 or 24 h later. Rats were killed 6, 24, 48 or 72 h after the operation. RESULTS: the TNF bioassay revealed high levels of TNF (30.2 +/- 5.4 U/ml, 35.0 +/- 5.0 U/ml and 36.6 +/- 6.0 U/ml) in the control group at 6, 24 and 48 h and (54.1 +/- 20 U/ml and 10.9 +/- 4.2 U/ml) in the pentoxifylline-treated group at 6 and 24 h, respectively, whereas the level had decreased to zero in the pentoxifylline-treated group at 48 h. The IL-6 bioassay likewise demonstrated high levels of IL-6 in the control group at 48 h and in the pentoxifylline-treated group at 6 and 24 h, and markedly decreased levels in the pentoxifylline-treated group at 48 h (7083 +/- 2844 pg/ml, 6463 +/- 1307 pg/ml, 10,329 +/- 5571 pg/ml vs 137.5 +/- 85.5 pg/ml, respectively, P < 0.05). The high mortality observed in the pancreatitis group (43%) was decreased by pentoxifylline administration to 11%. CONCLUSION: these results demonstrate that pentoxifylline very effectively inhibits cytokine production in acute pancreatitis.

Beneficial effect of octreotide treatment in acute pancreatitis in rats.

CONCLUSIONS: Octreotide treatment contributes to the regulation of tumor necrosis factor (TNF) production in sodium taurocholate-induced acute necrotizing pancreatitis in rats. Owing to its complex effect, octreotide can partially ameliorate the deleterious consequences of acute necrotizing pancreatitis. Elevated TNF and interleukin-6 (IL-6) levels in the peritoneal fluid may be considered a consequence of the activation of peritoneal macrophages. BACKGROUND: The effects of octreotide on exocrine pancreatic function have been investigated in numerous studies, but little attention has been paid to its influence on cytokine production in acute pancreatitis. METHODS: Acute pancreatitis was induced by the retrograde injection of taurocholic acid into the pancreatic duct in male Wistar rats. Serum amylase activity, wet pancreatic weight/body weight (pw/bw) ratio, and TNF and IL-6 levels were measured. Four micrograms/kg of octreotide was administered subcutaneously at the time of induction of pancreatitis and 24 or 48 h later. Rats were sacrificed 6, 24, 48, or 72 h after the operation. RESULTS: The serum amylase level and pancreatic weight to body weight ratio were decreased significantly in the octreotide-treated group. The serum TNF level was decreased significantly in the octreotide-treated group as compared with the control group at 6, 24, and 48 h (0.6 +/- 1.5, 2.0 +/- 3.3, and 0 vs 50 +/- 15.5, 37.5 +/- 18.4, and 13.1 +/- 12.5 U/mL, respectively). The ascites TNF level was decreased to 0 in the octreotide-treated group and was elevated in the control group at 72 h (28.0 +/- 49.0 U/mL). IL-6 production in ascites was extremely high in both groups at 6 h (80,000 +/- 43,817 pg/mL and 58,500 +/- 33,335 pg/mL), but the difference was not significant.

Plasma levels of TNF and IL-6 following induction of acute pancreatitis and pentoxifylline treatment in rats.

Activation of cytokine cascade is a decisive factor in determining the pathobiology of different inflammatory processes including acute pancreatitis. The purposes of this study were to determine the TNF and IL-6 levels after the induction of acute necrotizing pancreatitis, and to establish the effects of pentoxifylline on the cytokine production and the severity of pancreatitis. Acute necrotizing pancreatitis was induced by the retrograde injection of 200 microliters taurocholic acid into the pancreatic duct in male Wistar rats. TNF was titrated in a bioassay on cell line WEHI clone 164. IL-6 was measured via its proliferative action on the IL-6 dependent mouse hybridoma cell line B-9. Seven mg/kg pentoxifylline was administered intraperitoneally at the time of operation and/or 24 hours later. Rats were sacrificed, 48 or 72 hours after the operation. The TNF bioassay revealed high levels of TNF (36.6 +/- 6.0 U/ml) in the control group whereas levels decreased to zero in the pentoxifylline-treated group. The IL-6 bioassay likewise demonstrated high levels of IL-6 in the control group and markedly decreased levels in the pentoxifylline treated group (7083 +/- 2844 pg/ml, 6463 +/- 1307 pg/ml vs. 137.5 +/- 85.5 pg/ml, respectively, p < 0.05). The high mortality observed in the control group (43%) was sharply decreased by pentoxifylline administration to 11%. The data suggest that pentoxifylline is capable of modifying the cytokine production after 48 hours of induction of acute pancreatitis.